Long before posttraumatic stress disorder (PTSD) was a recognized psychiatric diagnosis, distressed trauma survivors complained about being easily startled (1
). As the diagnostic criteria for PTSD has evolved, “exaggerated startle” has remained a frequently endorsed symptom of the disorder (2
). Furthermore, PTSD has been associated with objective hyperstartle indicators such as larger eyeblink responses (the short latency primary index of human startle), larger electrodermal and cardiac responses (longer latency secondary startle responses), and slower habituation of electrodermal responses (a tertiary measure indexing reduced responding over repeated stimulus presentations) (3
). The primacy of the eyeblink response and the robustness of the secondary and tertiary measure findings (4
) justifies the continued examination of all of these measures in PTSD.
Exaggerated startle in PTSD was originally interpreted as resulting from either a proneness to excessive unconditioned responding to aversive stimuli (5
) or classical conditioning of traumatic experiences with coinciding startling sounds (e.g., gunfire). However, it became clear that PTSD patients do not show elevated reactivity to all aversive stimuli (7
) and that those exhibiting elevated startle reactivity have not necessarily experienced trauma involving loud sounds (3
). Recent thought posits that startle hyper-reactivity in PTSD is not an abnormal response to sudden intense stimuli but rather an augmented fear response to the context in which such stimuli occur. Though the startle reflex is implemented by a simple brainstem circuit, its magnitude and the magnitude of its secondary autonomic components may be potentiated by input from brain regions activated by threat cues and fear (8
). Under contextual threat
(i.e., settings in which the patient anticipates an aversive event), PTSD has been consistently associated with stronger startle eyeblink responding that appears to be independent of explicit threat cues (e.g., signals indicating precisely when the shock will occur) and relatively impervious to safety cues (e.g., signals indicating that the shock will not occur) (10
). Similar results have been observed for electrodermal responses to startling sounds (13
). However, in the absence of contextual threat, exaggerated eyeblink findings in PTSD have been less consistent (6
). Moreover, hypersensitivity to threatening contexts has been implicated in increased conditionability (i.e., more rapid learning and slower extinction of associations between previously neutral cues and aversive stimuli) (15
), which lends further plausibility to contextual threat sensitivity as a vulnerability factor for developing PTSD.
It is unknown, however, whether elevated startle responding is a pre-existing vulnerability factor for PTSD or is an acquired result of either trauma exposure or the development of other PTSD symptoms. Evidence has emerged on both sides of the argument. Orr et al. (16
) startled 130 Vietnam combat veterans and their non-combat exposed monozygotic twins and found that the veterans with PTSD exhibited greater heart rate responses to startling sounds than their non-exposed, genetically identical twin. This implied that the augmented heart rate responses were not pre-existing but rather acquired following trauma. Shalev et al. (17
) measured startle reactivity in 218 trauma survivors within one week of their trauma exposure and again four months later, at which time they were diagnosed with or without PTSD. The PTSD group showed no startle response differences one week after trauma but then demonstrated larger heart rate responses and slower eyeblink and skin conductance habituation four months later. Griffin (18
) found similar results in a study of 40 female interpersonal violence survivors who were exposed to startling sounds within one month post-trauma and then again at six months post-trauma when they were also diagnosed with or without PTSD. Neither initial eyeblink nor heart rate responses predicted later PTSD diagnoses but such diagnoses were accompanied by elevations in both physiological measures at the six month time point. These studies favor the view that abnormal startle responding is not a pre-existing vulnerability factor for PTSD but rather emerges along with PTSD symptoms, perhaps through a process of post-trauma progressive neuronal sensitization.
Yet, there are two important limitations to the aforementioned studies. First, none of them assessed startle prior to trauma exposure. Guthrie and Bryant (19
), on the other hand, measured startle-related eyeblink and skin conductance responses in firefighter trainees before they experienced duty-related trauma and found that both physiological measures prospectively predicted acute PTSD symptoms within 30 days of trauma exposure suggesting that startle may be a vulnerability factor. Second, no prospective study has manipulated contextual threat during startle assessment. If exaggerated startle actually indexes elevated fear due to contextual threat sensitivity then such threat might be necessary to reveal a prospective relationship between startle responses and PTSD. Therefore, it is unclear whether the Guthrie and Bryant results or previous failures to find a prospective relationship between startle and PTSD could be explained by the presence or absence of contextual threat.
The present study was undertaken to address both of these limitations by determining the relationship between pre-trauma startle reactivity under contextual threat and PTSD symptom severity after one year of exposure to police-related trauma. Contextual threat was established by warning cadets that they would receive a mild electric shock at a specific time during the study. Such uncontrollable but predictable aversive situations have been shown to increase generalized fear in animal models of PTSD (20
). The cadets were startled as their threat of being shocked was systematically increased. Exaggerated startle responses under low and medium threat of shock were conceptualized as primarily indexing contextual threat sensitivity. Exaggerated startle responses under high threat of shock were conceptualized as primarily indexing explicit threat sensitivity. We hypothesized that more severe PTSD symptoms at 12 months would be predicted primarily by contextual threat sensitivity and secondarily by explicit threat sensitivity. We also hypothesized that PTSD symptom severity would be predicted by slower habituation of startle responding (especially slower skin conductance habituation).